91.   It would be of scientific interest to know of plasma polyunsaturated fatty acids profile in inflammatory bowel disease as it might have both pathophysiological and therapeutic implications.

92.   The diagnosis of inflammatory bowel disease was based upon clinical, endoscopic and radiological findings and was supported by biochemical, scintigraphic and pathological features.

93.   Relatives of patients with inflammatory bowel disease were also excluded.

94.   This pattern of plasma fatty acids suggests that, in active inflammatory bowel disease, increased polyunsaturated fatty acid biosynthesis might coexist with increased fatty acid consumption.

95.   Two studies have shown that in inflammatory bowel disease the concentrations of arachidonic acid in the inflamed colonic mucosa were increased.

96.   According to this hypothesis, they have been administered in inflammatory bowel disease patients, but the results of various clinical trials are controversial.

97.   At concentrations found in the rectal lumen, the salicylates used in inflammatory bowel disease impair the binding of IFN to its receptor on colonic epithelial cells.

98.   Recent evidence favours the idea that inflammatory bowel disease may be caused by mesenteric vasculitis.

99.   Several different types of autoantibodies have been described in inflammatory bowel disease and primary sclerosing cholangitis.

100.   Wakefield et al presented evidence that vasculitis and microthrombosis in mesenteric vessels can be important pathogenetic factors in inflammatory bowel disease.